title: Gestational cadmium exposure-induced ovotoxicity delays puberty through oxidative stress and impaired steroid hormone levels.
abstract: Cadmium (Cd), an environmental pollutant, has been shown to be highly toxic to both humans and animals. Its widespread industrial use has led to its accumulation in the environment. Cd has been shown to target multiple organs following acute intoxication, causing nephrotoxicity, immunotoxicity, osteotoxicity, and reproductive toxicity. Cd can cross the placental barrier and cause a wide range of defects during fetal development. The current study was aimed to assess the effect of Cd on the female reproductive system. Female rats were exposed to Cd [50/200 ppm] from embryonic day 9 to 21 through drinking water. Serum steroid hormone concentrations, hematological parameters, antioxidant enzyme levels, and ovarian histopathology were described. Water consumption, gravid uterine/body weight decreased in both the doses of Cd-treated dams. The hematological parameters analyzed in rat pups showed a significant reduction in both doses of Cd studied, while hemoglobin showed a significant reduction in 200 ppm Cd treatment alone. MCHC levels did not show any variation in 50 ppm Cd treatment, while 200 ppm Cd treatment significantly increased. Specific activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione-S-transferase, and serum testosterone, estradiol, and progesterone were significantly decreased. The levels of hydrogen peroxide and lipid peroxidation were increased in 50 and 200 ppm Cd-treated rats. These changes were accompanied with disrupted ovarian histoarchitecture, an extended estrous cycle, and delayed pubertal onset in Cd-treated rats. The data generated from the present study suggest that gestational Cd treatment induces ovarian toxicity and reproductive dysfunction through increased oxidative stress.
authors.affiliation: Department of Zoology, St. John's College, Thirunelveli, TN, India. drbjsamuel@yahoo.co.in
authors.forename: Jawahar B
authors.initials: JB
authors.lastname: Samuel
authors.forename: Jone A
authors.initials: JA
authors.lastname: Stanley
authors.forename: Rajendran A
authors.initials: RA
authors.lastname: Princess
authors.forename: Paulraj
authors.initials: P
authors.lastname: Shanthi
authors.forename: Maria S
authors.initials: MS
authors.lastname: Sebastian
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001772:Blood Cell Count; D001835:Body Weight / Q000187:drug effects; D002104:Cadmium / Q000633:toxicity*; D004798:Enzymes / Q000097:blood; D030762:Estrous Cycle / Q000187:drug effects; D005260:Female; D006728:Hormones / Q000097:blood*; D006861:Hydrogen Peroxide / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D009929:Organ Size / Q000187:drug effects; D010049:Ovarian Diseases / Q000139:chemically induced* / Q000473:pathology; D010053:Ovary / Q000187:drug effects / Q000254:growth & development / Q000473:pathology; D018384:Oxidative Stress / Q000187:drug effects*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D011863:Radioimmunoassay; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D012098:Reproduction / Q000187:drug effects; D012741:Sexual Maturation / Q000187:drug effects*; D013256:Steroids / Q000097:blood*
chemical_list: D000975:Antioxidants; D004798:Enzymes; D006728:Hormones; D017382:Reactive Oxygen Species; D013256:Steroids; D002104:Cadmium; D006861:Hydrogen Peroxide